Despite the development of regional trauma centers, improved emergency transport systems to reduce the total time in shock, and aggressive resuscitation treatments, trauma patient mortality and morbidity remains high. Traumatic injury is the leading cause of death in subjects <44 years of age, resulting in over 150,000 deaths annually. Severe hypovolemia due to hemorrhage is a major factor in nearly half of those deaths. Furthermore, patients who survive the initial injury are at a high risk of developing subsequent multiple organ dysfunction syndrome and sepsis with a significant rate of late mortality in the ICU. More effective patient monitoring technology would identify patients at risk to develop organ failure and guide appropriate therapy.
Current monitoring required to assess hemodynamic function is often invasive and is limited to high acuity settings. Non-invasive monitoring conducive to lower acuity settings (i.e., areas of care where invasive and cumbersome monitoring techniques cannot be practically implemented) currently provides static, unidimensional, and isolated information of questionable utility.
Severe shock associated with trauma is characterized by a decreased circulatory blood flow that does not meet the metabolic demands of the body. Shock is the result of a vast array of processes with different time courses, degrees of cardiovascular compensation, monitoring needs, pathophysiologies, treatments, and outcomes. However, in all cases, prolonged and unrecognized impaired tissue perfusion will cause organ injury, increased morbidity, and death. Circulatory shock occurs from any of a variety of causes, but has as its hallmark inadequate tissue perfusion such that ischemic dysfunction and organ injury inevitably develop. If tissue hypoperfusion is not reversed by intravascular fluid resuscitation and/or pharmacologic support aimed at restoring normal cardiac performance and vasomotor tone, organ failure and death occur. However, only half of the patients with cardiovascular insufficiency increase their cardiac output in response to volume loading. Thus, it is important to identify which patients are preload-responsive (i.e. they will increase their cardiac output in response to fluid resuscitation) because giving fluid resuscitation to a patient who is not preload-responsive will not improve their circulatory status and delays effective treatment. Delaying treatment results in organ injury and intravascular volume overload, which induces acute right ventricular failure (acute cor pulmonale) and pulmonary edema, both of which can compromise normal homeostatic mechanisms and induce circulatory shock and death.
The prior art has at least three major deficiencies. First, the devices available to monitor a patient's systemic stability are quite insensitive. Second, the mechanisms for monitoring such patients requires that patients are either mechanically ventilated or are in an environment in which only crude maneuvers may be implemented to perturb the cardiovascular system, such as by raising a leg or abdominal compressions. Finally, the output generated by currently available devices requires skilled care providers to interpret the output and to decide appropriate actions or treatment protocols.
Thus, there is a need for a device that can transform insensitive signals into something meaningfully related to the subject's systemic state. There is also a need for a method that can be implemented in a spontaneously breathing subject and/or avoids the inconvenience of physical maneuvers to perturb the cardiovascular system. Finally, there is a need for a device that can be used by a less skilled care provider, such as emergency response personnel, so that critically ill patients receive effective treatment quickly.